Indian Institute of Technology Bombay

Topological quantum materials offer new levers for thermoelectric (TE) design by reshaping band geometry, carrier scattering, and heat transport. This review provides a unified account of these opportunities from three complementary perspectives. First, we develop an analytical framework based on the Bernevig-Hughes-Zhang model, which makes explicit how Berry curvature, entropy, and chemical potential jointly control the anomalous Nernst response across trivial, critical, and topological regimes. Within a Landauer-Büttiker picture, we show how helical edge channels can act as nearly ideal step-like energy filters when transmission is engineered to be strongly energy dependent, clarifying that topological protection alone yields vanishing thermopower and that sizeable Seebeck and Nernst signals require controlled particle-hole asymmetry without sacrificing conductance. Second, we survey material platforms where these mechanisms are realized or anticipated: three-dimensional topological insulators and quantum spin Hall monolayers such as jacutingaite, Dirac and Weyl semimetals, goniopolar and magnetic topological semimetals, altermagnets, and systems hosting topological magnons and phonons. Particular emphasis is placed on the interplay of band inversion, spin-orbit coupling, magnetism, and lattice thermal conductivity, as well as on transverse Nernst and Ettingshausen geometries. Finally, we review emerging machine-learning strategies for topological TEs, covering data curation, descriptor engineering, tree-based and neural-network models, graph-based approaches, active-learning loops, and literature mining workflows that directly target power factor and figure of merit. Together, these analytical, materials, and data-driven perspectives outline design principles and computational pathways for exploiting topology as a controllable resource in next-generation TE materials and devices.

Abstract Aging causes a progressive loss of tissue homeostasis, with stem cell exhaustion as a major hallmark. Age-associated decline in organ function is widely perceived as emanating from progressive accumulation of cellular damage in adult tissues. However, whether aging trajectories are established early on during development remains an open question. Here, we demonstrate that genetic modulation of cellular aging pathways in larval adult midgut progenitors (AMPs), which serve as the precursors of adult intestinal stem cells and differentiated epithelial cells, dictates the long-term trajectory of intestinal aging in Drosophila . Accelerated cellular aging by genetic perturbation employing Toll or Imd pathway overactivation or elevation of reactive oxygen species (ROS) using ND42 (mitochondrial complex I) knockdown in the AMPs results in aberrant progenitor proliferation, skewed lineage allocation, epithelial barrier dysfunction, and genomic instability. These alterations are accompanied by marked destabilization of AMP islet architecture and widespread changes in age-related molecular signatures, as revealed by bulk transcriptomic analysis. In contrast, decelerated cellular aging mediated by Foxo or Atg8a overexpression results in a decrease in enteroendocrine population and the intestinal barrier remained unaffected. Intriguingly, early-life activation of immune and oxidative stress signaling manifested later in the adult gut as elevated enteroendocrine differentiation, highlighting lasting effects on intestinal regenerative capacity and lineage balance. Together, our findings demonstrate that cellular aging is tightly regulated early on in development and its perturbation can cause developmental disruption hampering adult gut homeostasis, establishing AMPs as key developmental determinants that regulate the trajectory of intestinal aging in Drosophila .